Lipid Metabolism Bullshit Flashcards
1
Q
Lipids are ___phobic compounds but soluble in _______
A
hydro
organic solvents
2
Q
Major lipids in plasma include fatty acids, triglycerides, cholesterol, phospholipids,__________
A
Terpenes (Vitamins A,E,K)
3
Q
Increased level of lipids in blood is often associated with ______ diseases which can lead to death
A
cardiovascular
4
Q
Lipids contained in plasma exist and are transported in the form of _________
A
lipoprotein
5
Q
Liproproteins are (Covalent or Non-covalent?) assemblies of ____ and ____
A
Non-covalent
lipids and proteins
6
Q
Structure of liproproteins
Core - _______ and ______
Surface – _____, Proteins and __________ and proteins
A
Triglycerides and Cholesterol esters
Phospholipids
cholesterol esters
7
Q
Triglycerides are found in ____
A
diet
8
Q
Triglycerides can not be synthesized in the liver
T/F
A
F
It can
9
Q
Classification of lipoproteins
Based essentially on _______ determined by ______
A
densities
ultracentrifugation
10
Q
Classification of liproproteins
Density increases from _______ through lipoproteins of _________, _________ and ___________ , to _________
A
chylomicrons (CM, of lowest density)
very low density (VLDL), intermediate density (IDL)
low density (LDL)
high density lipoproteins (HDL).
11
Q
The composition of the circulating lipoproteins is static.
T/F
A
F
not static
12
Q
Circulating liproproteins are in a dynamic state with continuous exchange of components between the various types
T/F
A
T
13
Q
Lipoprotein(a), or Lp(a), is a normal lipoprotein of known function.
T/F
A
F
atypical
Unknown function
14
Q
LpA
is (smaller or larger?) and (more or less ?) dense than LDL but has a (different or similar?) composition, except that it contains in addition _________________
A
Larger
More
Similar
one molecule of apo(a) for every molecule of apo B-100.
15
Q
Apo(a) shows considerable homology with ________.
A
plasminogen
16
Q
The concentration of Lp(a) in the plasma varies considerably between individuals, ranging from _____ to _______ mg/L.
A
0 to 1000
17
Q
An elevated concentration of Lp(a) appears to be a/an (dependent or independent?) risk factor for CHD.
A
Independent
18
Q
• Chylomicrons
• Chylomicrons are formed from ________ (principally ______ and ______ ) in enterocytes
A
dietary fat
triglycerides,
and cholesterol
19
Q
Chylomicrons
They reach the systemic circulation via the ______
A
thoracic duct
20
Q
________ are the major transport form of dietary fat.
A
Chylomicrons
21
Q
Triglycerides constitute about ___% of the lipid in chylomicrons
A
90
22
Q
Triglycerides are removed from chylomicrons by the action of the enzyme _______, located on the ________ surface of the capillary endothelium of ____ tissue, ____ and _____muscle and ________, with the result that ______ are delivered to these tissues to be used either as _______ or, after re-esterification to triglyceride, for _______.
A
lipoprotein lipase (LPL)
luminal
adipose
skeletal and cardiac ; lactating breast
free fatty acids; energy substrates
energy storage
23
Q
LPL is activated by _____
A
apo C-II
24
Q
Apo A and apo B-48 are synthesized in the ____
A
intestine
25
Apo A and apo B-48 are present in newly formed chylomicrons
T/F
T
26
_____ and _____ are transferred to chylomicrons from HDL.
Apo C-II and apo E
27
As triglycerides are removed from chylomicrons by the action of ____, these become (smaller or larger?)
______,_______,_______,________ are released from the surface of the particles and taken up by ______
LPL
Smaller
cholesterol, phospholipids, apo A and apo C-II
HDL.
28
The chylomicron remnants, depleted of ______ and enriched in ________ are cleared rapidly from the circulation by hepatic?
Triglyceride
cholesteryl esters,
29
Chylomicron major function is the transport of ________
dietary triglyceride
30
chylomicrons also transport dietary cholesterol and fat-soluble vitamins to the liver.
T/F
T
31
Under normal circumstances, chylomicrons cannot be detected in ____ in the ______ state (>___ h after a meal).
plasma
fasting
12
32
Very low density lipoproteins(VLDL)
VLDL are formed from _____ synthesized in the ____ either ____ or by ______ of ______
triglycerides; liver
de novo
re-esterification of free fatty acids.
33
VLDL also contain some ______,_______,______,______
cholesterol, apo B, apo C and apo E
34
VLDL
the apo ___ and some of the apo __ is transferred from circulating ____.
E; C
HDL
35
VLDL
Cholesterol, phospholipids and apo C and apo E are released and transferred to ______.
HDL
36
VLDL
Triglycerides are removed by _______ and is thereby converted into _____.
hepatic triglyceride lipase
LDL
37
Triglyceride-rich VLDL are precursors of ___, which comprise mainly ______ and ______
LDL
cholesteryl esters and apo B-100.
38
Very low density lipoproteins(VLDL)
•VLDL are the principal transport form of ________ and initially share a similar fate to _______
endogenous triglycerides
chylomicrons
39
As the VLDL particles become smaller, phospholipids, free cholesterol and apolipoproteins are released from their surfaces and taken up by ____
HDL
40
IDL
More ____ are removed by ______, located on hepatic endothelial cells, and IDL are thereby converted to ____.
triglycerides
hepatic triglyceride lipase
LDL
41
Hepatic receptors, also known as ___,____ receptors, are capable of binding _______ and ______ (but not ________).
B, E
apo B-100 and apo E
apo B-48
42
Low density lipoproteins (LDL)
• LDLs are the principal carriers of ______, mainly in the form of _____
cholesterol
cholesteryl esters.
43
LDL are formed from _____ via _____.
VLDL via IDL
44
LDL can pass through the junctions between _________ and attach to LDL receptors on ________ that recognize apo _____.
This is followed by ______ and ———- with release of ________
capillary endothelial cells
cell membranes
B-100
internalization and lysosomal degradation
free cholesterol
45
LDL is removed by the _____ and other tissues by a _____- dependent process involving the recognition of ______ by the LDL receptor.
liver
receptor
apo B-100
46
LDL receptors are not saturable
T/F
F
47
LDL receptors are subject to down-regulation
T/F
T
48
Macrophages derived from circulating monocytes can’t take up LDL
T/F
F
They can
49
Uptake of LDL by macrophages in the arterial wall is an important event in the pathogenesis of _______.
atherosclerosis
50
When macrophages become overloaded with _______, they are converted to ____ cells, the classic components of __________
cholesteryl esters
foam
atheromatous plaques.
51
High density lipoproteins(HDL)
HDL are synthesized primarily in the ___ and, to a lesser extent, in ______ cells, as a precursor (‘ _________ ’) comprising phospholipid, cholesterol, ______,——
liver
small intestinal
nascent HDL
apo E and apo A.
52
Nascent HDL is ____ shaped
disc
53
HDL
In the circulation, it acquires apo ___ and apo __ from ______ and from extrahepatic tissues, and in doing so assumes a _______ conformation.
C; A
other lipoproteins
spherical
54
HDL
The free cholesterol is esterified by the enzyme ________________ , which is present in ____ and activated by its cofactor, apo ___. This increases the ____ of the HDL particles, which are thus converted from _____ to ____
lecithin-cholesterol acyltransferase (LCAT)
nascent HDL
A-I
density; HDL3 to HDL2.
55
HDL metabolism and reverse cholesterol transport
• Cholesterol in nascent HDL is esterified by _____
LCAT
56
Reverse cholesterol transport
Cholesteryl esters are transferred from ___ in exchange for ______, this process being mediated by ____________ protein.
HDL
triglycerides
cholesteryl ester transfer
57
Cholesteryl esters are taken up by the liver in _____ and _____.
The triglyceride-enriched HDL2 are converted to HDL3 by ___________ by the enzyme _________, located on the hepatic capillary
chylomicron remnants and IDL
the removal of triglycerides
hepatic triglyceride lipase
58
HDL has two important functions
• it is a ____ of _________ for ______
• mediates ___________
source; apoproteins for chylomicrons and VLDL
reverse cholesterol transport
59
reverse cholesterol transport is basically taking up of cholesterol from _____ cells and _______ and transferring it to _______, which are taken up by the _____.
senescent
other lipoproteins
remnant particles
liver
60
The essential features of lipoprotein metabolism are as follows
• Dietary triglycerides are transported in ______ to ____ where they
can be used as an _____ or ____
• Endogenous triglycerides, synthesized in the _____, are transported in ___ and are also available to _____ as ______ or for __________
chylomicrons; tissues; energy source or stored
liver; VLDL; tissues; an energy source or for storage
61
The essential features of lipoprotein metabolism are as follows
• cholesterol synthesized in the ____ is transported to tissues in ___, derived from _____ via ____
• Dietary cholesterol reaches the liver in __________
• HDL acquire cholesterol from _______ and other
liver; LDL; VLDL; LDL
chylomicron remnants
peripheral cells
62
Disorders of lipid metabolism
• There are several rare, inherited metabolic diseases associated with the accumulation of lipids in tissues (______________ which can be primary or secondary), and others in which plasma lipoprotein concentrations are reduced
Hyperlipidaemias
63
Primary Hyperlipidaemia
Familial hypercholesterolaemia (FH)
Common’ (polygenic) hypercholesterolaemia
Familial dysbetalipoproteinaemia
Familial chylomicronaemia
Familial hypertriglyceridaemia
Familial combined hyperlipidaemia
Familial hyperalphalipoproteinaemia
64
Familial hypercholesterolaemia (FH)
This condition is characterized by high plasma ______ concentrations that are present from ———- and do not depend on the _______________
cholesterol
early childhood
presence of environmental factors
65
Familial hypercholesterolaemia (FH)
• It is inherited as an autosomal _______ characteristic.
Different mutations can affect _________ synthesis, transport, ligand binding, clustering in coated pits and recycling, but all cause a similar phenotype
dominant
LDL receptor
66
Familial hypercholesterolaemia (FH)
• Familial defective_______, in which a mutation in the ______ decreases the ___________, causes a similar phenotype.
apo B-100
apo B gene
avidity of LDL for its receptor
67
Familial hypercholesterolaemia (FH)
In all cases, there is a defect in the _____________, and its plasma concentration is increased. In heterozygotes, total cholesterol is typically in the range 7.5–12 mmol/L. The diagnosis is based on the presence of hypercholesterolaemia (>7.5 mmol/L in adults
uptake and catabolism of LDL
68
In FH
• There is usually tendon _______ in the individual or close relative, or on DNA evidence of a recognized mutation.
xanthomata
69
‘Possible’ FH is considered to be present in patients who do not meet these definitive criteria, but who _________________________ together with ___________________
have the same degree of hypercholesterolaemia
a family history of premature CHD or hypercholesterolaemia.
70
Common’ (polygenic) hypercholesterolaemia
• The distribution of plasma cholesterol concentrations in relatives is _____
• More frequently, when the family of an individual with hypercholesterolaemia is studied, a ___________ is found, consistent with the ________ being influenced by _______.
This entity has been termed ‘ _______ ’ or ‘_____’ hypercholesterolaemia
bimodal
continuous distribution
plasma cholesterol; several genes
common; polygenic
71
Difference between familial hypercholesterolemia and Common’ (polygenic) hypercholesterolaemia
Plasma cholesterol in common is not generally as high as in FH
Common is more influenced by environmental factors
72
Common’ (polygenic) hypercholesterolaemia
The significance of this condition again lies in its relationship to the risk of _________, and the principles of management are (similar or different ?) to those for FH.
coronary artery disease
Similar
73
common (polygenic) hypercholesterolaemia
In polygenic hypercholesterolaemia, however, _________ alone may sometimes be adequate to lower the cholesterol concentration to acceptable levels.
dietary treatment
74
Familial dysbetalipoproteinaemia
• This condition is characterized clinically by the presence of ______ in the _________ and by ________
the latter tend to occur over ________ and, unlike tendon xanthomata, are _____ in colour.
Fat deposits ; palmar creases
tuberous xanthomata
bony prominences ; reddish
75
Familial dysbetalipoproteinaemia
• In some patients, ______ xanthomata are present
• Biochemically, the condition is characterized by the presence of an excess of ______ and ______
_______ are sometimes also present.
eruptive
IDL and chylomicron remnants
chylomicrons
76
Familial dysbetalipoproteinaemia
Total cholesterol and triglyceride concentrations are ______, typically to ________ values.
elevated
approximately equal
77
Familial dysbetalipoproteinaemia
Patients have increased risk of _______________________ disease
both coronary and peripheral Cardiovascular
78
Familial chylomicronaemia
• Fasting chylomicronaemia is a feature of two rare hyperlipidaemias, both having an autosomal ______
• deficiency of the enzyme _____
• deficiency of ______, which is required for activation of this enzyme
• The result in each case is a failure of _________ from the bloodstream.
recessive
lipoprotein lipase
apo C-II
chylomicron clearance
79
Familial chylomicronaemia
• Presentation is usually in _____, with _____ xanthomata, recurrent abdominal pain due to _______ and sometimes ______.
childhood
eruptive
pancreatitis
hepatosplenomegaly
80
In Familial chylomicronaemia Lipaemia retinalis may also be present.
T/F
T
81
Familial chylomicronaemia
• Management involves giving a _______, with substitution of some fat by ______
low fat diet
triglycerides
82
Familial hypertriglyceridaemia
• This condition is usually associated with an excess of ______ in plasma.
It is usually not manifest until ______.
VLDL
adulthood
83
Familial hypertriglyceridaemia
The molecular basis is uncertain; there is increased hepatic synthesis of ______.
Inheritance is autosomal ______.
VLDL
dominant
84
Familial hypertriglyceridaemia
Triglyceride concentrations are not usually higher than ___ mmol/L,
5
85
Familial combined hyperlipidaemia
• This is due to hepatic overproduction of _____, leading to increased ____ secretion and increased production of __________.
Either _______ or _______ , or both, may be elevated
apo B; VLDL
LDL from VLDL
plasma cholesterol or triglyceride
86
Familial combined hyperlipidaemia
• Hyperlipidaemia with increased risk of coronary artery disease is usually present
T/F
T
87
Familial hyperalphalipoproteinaemia
• Hypercholesterolaemia is due to an increase in only the _____ fraction, which may be present in other members of the family
• CHD risk may be ___eased, and _________ treatment is required
HDL
decr
no specific
88
Familial hyperalphalipoproteinaemia
The existence of this condition underlines the need to measure _________ in patients with hypercholesterolaemia.
Generally, if total cholesterol is greater than 7 mmol/L, there will always be an increase in _____, but, even then, measurement of _____ helps in the assessment of CHD risk
HDL cholesterol
LDL
HDL
89
The management of lipid disorders
Essentials of management is based on
• Adequate ______
•______ modification
• Use of drugs like _______,_______,________
• Proper management of _________ that increaser risk of CVD eg, ____
risk assessment
Lifestyle
statins, HMG co A reductase inhibitor, fibrates
Secondary conditions; DM
